The host cell has been generally considered a passive bystander in the infectious process. Recent developments however point to the fact that there is a dynamic interaction between infectious agents and the host cell, influencing each others physiological responses. Indeed, it has been now demonstrated that some nonviral infectious disease agents modulate biological host cell processes such as apoptosis and may even contribute to malignant transformation of the host cell. Interestingly, number of sexual contacts and inflammation have been identified as contributing factor in cervical and prostate cancers.Cervical cancer is the most common gynecological malignancy and the second leading cause of death in women worldwide. In men, prostate cancer is the most common diagnosed cancer and second leading cause of death in the USA. Minority population bear an disproportinate burden of these cancers. Furthermore, the etiology of both cancers have not been completely iluminated and epidemological studies suggest that STI such T. vaginalis may be co-factors in these malignancies. Our goal is to unravel the molecular basis of the association of cervical and prostate cancers and trichomonosis.The hypothesis to be tested is that chronic infection of the prostate and cervical epithelium by trichomonad parasites initiates, augments, and/or maintains the type of biological alterations that promotes the development and progression of cervical/prostate cancer. The longterm objective of this work is to demonstrate that trichomonad prostatitis and cervicitis in which trichomonads alter the host environment contributes to neoplasia. To accomplish this goal and test the hypothesis five specific aims are proposed that examine the molecular alteration in the physiology and gene expression patterns of host cells due to the intimate contact with tricdhomonads. It is anticipated that ourfindings will provide a new direction for screening and treatment of this STD, which will decrease the incidence of cancer among our citizens.